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Differential complementation of Bcr-Abl point mutants with c-Myc.
A complementation strategy was developed to define the signaling pathways activated by the Bcr-Abl tyrosine kinase. Transformation inactive point mutants of Bcr-Abl were tested for complementation with c-Myc. Single point mutations in the Src-homology 2 (SH2) domain, the major tyrosine autophosphorylation site of the kinase domain, and the Grb-2 binding site in the Bcr region impaired the transformation of fibroblasts by Bcr-Abl. Hyperexpression of c-Myc efficiently restored transformation activity only to the Bcr-Abl SH2 mutant. These data support a model in which Bcr-Abl activates at least two independent pathways for transformation. This strategy may be useful for discerning signaling pathways activated by other oncogenes.[1]References
- Differential complementation of Bcr-Abl point mutants with c-Myc. Afar, D.E., Goga, A., McLaughlin, J., Witte, O.N., Sawyers, C.L. Science (1994) [Pubmed]
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